Normal Joint Function
The anatomy of the normal joint demonstrates articular cartilage on subchondral bone. The two cartilage surfaces oppose each other. The synovial tissue around the joint produces joint fluid, which lubricates the joint and nourishes the cartilage.
The ligaments that surround the joints provide stability to the joints. Normal joint motion occurs when the two cartilage surfaces glide across each other in both rotation and translation. The cartilage is made up of chondrocytes, which are the cartilage cells and extracellular matrix. The extracellular matrix is composed of type 2 collagen and proteoglycans. Proteoglycans are large sulfated sugar molecules. Both components are produced by the chondrocytes. The function of these large proteoglycan molecules is that they attract water molecules through their negatively charged sulfur ions, which attract the positive hydrogen atom of the water dipole. The collagen gives the cartilage tensile strength which resists shear forces. The proteoglycans allow cartilage to absorb water by ionic attraction and osmotic gradients. Cartilage also imbibes water through flexion and extension of the joint. As a result, cartilage is a highly specialized tissue with characteristics to absorb compressive forces and resist tensile forces. The subchondral bone provides support to the articular cartilage and blood supply to the deeper cartilage layers. Histologically, articular cartilage has 4 layers: superficial layer, transitional layer, radial layer and calcified layer. Each layer has a characteristic morphology and function. (Ref 1).
Pathological Degenerative Arthritis
When the articular cartilage structure is maintained normal joint function occurs. When the articular cartilage degenerates joint function is compromised. The stages of degeneration are initiated by an insult such as a traumatic event or through gradual degeneration and mechanical wear over time. Biochemically the initiating factors are the release of chemotactic factors by the chondrocytes and synovial tissue such as IL-1, and TNF, which attract white blood cells such as leukocytes and macrophages into the region. These white blood cells release enzymes such as metalloproteinases which degrade collagen and proteoglycans. (Ref. 1, Ref. 2). In addition, chondrocytes release these degradative enzymes into the extracellular matrix further degrading the cartilage. As the proteoglycans break down, the cartilage has less ability to hold water. As a result, the cartilage has less ability to resist compressive forces. As the collagen gets degraded, the cartilage has decreased ability to resist tensile forces. As the process progresses, increased degradation and mechanical wear of the articular cartilage occurs resulting in degenerative osteoarthritis. (Ref. 1, Ref 2) The cartilage surface becomes thinner until there is bone on bone contact. During the degenerative process the synovial fluid becomes thinner and the bone edges of the joint form osteophytes in an attempt to stabilize the joint. As the joint continues to deteriorate, the patient clinically has increased swelling, pain, loss of motion and loss of function.
Many musculoskeletal diseases lead to joint damage and degenerative arthritis such as trauma and fractures that heal malaligned, infection that damages the joint surface, inflammatory arthritis such as rheumatoid arthritis that has hypertrophic synovium that damages the cartilage surface. (Ref. 1).
Treatment options for degenerative osteoarthritis range from conservative to surgical depending on the disease severity. Conservative treatment includes rest, NSAID, braces etc. Hyaluronic gel injections provide good relief of symptoms for significant period of time by replacing the thin synovial fluid with hyaluronic gel that is similar in viscosity to normal synovial fluid. The gel lubricates the joint and provides an anti-inflammatory effect. If conservative treatment fails and the patient becomes increasingly symptomatic, then surgical treatment is instituted. Surgical options include arthroscopy and debridement, open debridement, osteotomy, arthrodesis and joint replacement arthroplasty. (Ref. 3). Arthroscopy and joint debridement are indicated for early degenerative arthritis. Arthrodesis is for more advanced degeneration. The purpose of arthrodesis surgery is to remove the involved degenerative joint surfaces. Then the joint is made stiff by bridging the 2 bone ends together with internal fixation such as plate and screws or external fixation. This eliminates motion and providing a stable joint region. As a result, pain is removed and function is improved. (Ref 4). Fusion can be done for any arthritic joint and common joints that are fused are spine vertebral joint segments, ankle and feet, wrist and hands, etc. (Ref. 5)
The disadvantages of arthrodesis surgery are that motion is lost in the fused joint. A joint can take from 2-4 months to heal. In addition complications of arthrodesis are non-union, or implant failure. (Ref 4). Arthrodesis of spinal segments can be especially problematic and even with newer instrumentation, fusion failure occurs. Also, once the joint is fused stiff there is no motion and the stress is transferred to adjacent joints, and these joints may eventually deteriorate.
The most common surgical treatment for degenerative arthritis of joints is joint arthroplasty or joint replacement. (Ref 6, Ref. 7, Ref. 8). The most common joint replacements performed are total hip and total knee replacements. Other joint replacements performed are finger joint replacements, elbow joint replacements, wrist replacements and shoulder replacements. (Ref. 5, Ref. 9, Ref. 10, Ref. 11). The introduction and refinement of total joint replacements has been one of the great advances in orthopedic surgery. (Ref. 8). The advantages of total joint replacements are that an arthritic joint that has poor motion and function and which causes significant pain and discomfort can be replaced with metal and polyethylene, eliminating pain and increasing motion and function. Total hip replacements have been performed extensively to replace degenerated hips. They have been widely successful eliminating pain and increasing function. The life span for a total hip replacement can average between 20-30 years. (Ref. 6, Ref 7, Ref. 8).
Total hip replacements are placed by removing the arthritic femoral head and placing a metallic or ceramic femoral component which has a head portion and a stem portion that is fixated into the femoral canal by press or interference fit or with cement. The degenerated acetabulum is removed and a metal or ceramic cup or socket is placed into the acetabulum and fixated by press or interference fit or stabilized with cement or screws. A polyethylene liner is placed in the cup as the articulating surface for the head of the femoral component. Once the components are in place the femoral component is reduced into the acetabular component. Stability of the prosthesis through a range of motion is obtained by the congruent fit of the head portion of the femoral component and the cup component of the acetabulum, the correct alignment and positioning of the components, and the tension obtained of the soft tissues such as the muscles, ligaments and tendons around the components. (Ref 8, Ref 12).
Most total hip replacements are placed using a posterior approach from the back of the hip. This approach is more commonly used due to the fact that visualization of the hip is improved. Going posteriorly, however, has a higher dislocation rate (Ref 12, Ref. 13), as this approach results in the posterior capsule or ligaments being removed to place the prosthesis. To protect the hip from dislocating total hip precautions are instituted post operatively. Positions of hip adduction and hip flexion and internal rotation put the greatest stress on the prosthesis and can result in dislocation posteriorly. (Ref 12).
The vast majority of total hip replacements are successful. (Ref. 7). Complication of total hip replacements do occur, however, and the most common complications are loosening of the prosthesis, dislocation and infection. (Ref 12). Dislocation of the hip is the second most common complication. (Ref. 14). In one study, e.g., approximately 4% of total hip replacements performed using a posterior approach resulted in dislocation. (Ref. 13). Causes of total hip dislocation are surgical factors such as improper placement of the components, patient factors such as poor soft tissue tension and poor patient compliance, or prosthesis factors. (Ref. 13, Ref 15). The patients place the leg in an adducted or leg crossing over position and hyperflexion of the hip. This position places the greatest strain on the hip and leads to dislocation posteriorly or out the back of the acetabular cup. (Ref. 12).
Treatment
Treatment for total hip dislocations includes placing the dislocated femoral head back into the acetabular cup manually under anesthesia. (Ref. 9). The patient is placed in a brace and the hip kept from going into positions that place it at risk of re-dislocating until the soft tissues re-tighten. Once a patient dislocates a total hip replacement, they are at greater risk of re-dislocating in the future. If re-dislocation occurs the replacement and adjustment of component position may be necessary. (Ref. 12). If re-dislocation continues to reoccur then placement of a constrained prosthesis may be necessary. (Ref. 16, Ref. 17). Once total hip dislocations occur there is a risk of multiple surgeries and poorer final functional outcome for the patient. (Ref 12).
Janssen et al. U.S. Pat. No. 4,024,588 describes artificial joints wherein a permanent magnetic field is created between two components for attraction or repulsion by placing permanent magnets in both components of the total joint prosthesis. They specifically demonstrate this for a multitude of joint replacements including total joint replacements in which femoral and acetabular components have magnets. Bertram US. 2003/0236572 further describes total joint replacements using magnetism to control instability. While magnet placements are described in such references which allow translation in various joints while providing increased stability, there is no disclosure regarding placements of magnets of varying strength in joints to decrease risk of dislocation, and in particular to prevent hip dislocations posteriorly, while also reducing the risk of component loosening due to strength of the magnetic fields.
Hyde, Jr. U.S. Pat. Pub. No. 2002/0128651 describes apparatus and methods for stabilizing and/or maintaining adjacent bone portions in predetermined desired relationships and for constraining one, two or three dimensional motion and/or rotation of the adjacent bone portions wherein implanted magnetic arrays provide interacting magnetic fields in the area of the bone portions. While magnet placements are described which generate interacting magnetic fields in an articular joint to reduce the joint reactive forces while constraining the bone portions to move in a natural joint motion, there is again no disclosure regarding placements of magnets in joints to decrease risk of dislocation, and in particular to prevent hip dislocations posteriorly, while also reducing the risk of component loosening due to strength of the magnetic fields.